Low levels of CC16 in nasal fluid of children with birch pollen-induced rhinitis
Version of Record online: 6 APR 2005
Volume 60, Issue 5, pages 638–642, May 2005
How to Cite
Johansson, S., Keen, C., Ståhl, A., Wennergren, G. and Benson, M. (2005), Low levels of CC16 in nasal fluid of children with birch pollen-induced rhinitis. Allergy, 60: 638–642. doi: 10.1111/j.1398-9995.2005.00775.x
- Issue online: 6 APR 2005
- Version of Record online: 6 APR 2005
- Accepted for publication 27 September 2004
- allergic rhinitis;
- Clara cell;
- secretoglobin 1a1
Background: Clara cell protein 16 (CC16; secretoglobin 1A1) is an anti-inflammatory protein mainly expressed in the epithelial cells in the airways.
Objective: To compare the levels of CC16 in nasal lavage (NAL) from children with intermittent allergic rhinitis and healthy controls and to study the effect of a local steroid.
Methods: Thirty schoolchildren with birch pollen allergy and 30 healthy controls from the same schools were included in the study. The NAL fluid was collected before the season, during the birch pollen season and, for the patients, after 1 week of treatment with a local steroid. Symptom scores were obtained on every occasion. CC16 and eosinophil cationic protein (ECP) were analyzed with enzyme-linked immunosorbent assay.
Results: The nasal fluid levels of CC16 were significantly lower in patients than in controls, before and during pollen season. Before the season, the median CC16 concentrations were 9.1 (range 1.1–117) μg/l in patients and 25.7 (6.1–110.2) μg/l in controls. During the season, the median CC16 concentrations in nasal fluid were 12.9 (2.3–89.7) μg/l in the allergic children and 22.0 (9.5–90.1) μg/l in the healthy controls (P = 0.0005). Symptom scores, nasal fluid eosinophils and ECP were higher in patients during the season. Treatment with a local steroid did not change the CC16 levels.
Conclusions: Nasal fluid CC16 levels were lower in children with birch pollen-induced allergic rhinitis than in healthy controls both before and during the pollen season. We speculate that reduction in anti-inflammatory activity by CC16 may contribute to the pathogenesis of allergic rhinitis.